Correction: Hu, W., et al. Targeting Dopamine Receptor D2 by Imipridone Suppresses Uterine Serous Cancer Malignant Phenotype. Cancers 2020, 12, 2436

Hu, Wen; Zhang, Li; Ferri-Borgogno, Sammy; Kwan, Suet-Ying; Lewis, Kelsey; Cun, Han; Yeung, Tsz-Lun; Soliman, Pamela T.; Tarapore, Rohinton; Allen, Joshua E.; Guan, Xin‐Yuan; Lu, Karen H.; Mok, Samuel C.; Au-Yeung, Chi-Lam

doi:10.3390/cancers13040623

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“…ONC201 is currently in phase I/II clinical trials ( 13 ) as an antitumor therapeutic agent for several human cancers including neuroendocrine tumors and recurrent glioma (e.g., Clinicaltrials.gov NCT03034200). ONC206 has shown great promise in pre-clinical models including glioblastoma ( 10 ), high-grade gliomas, medulloblastomas, neuroblastomas, sarcomas ( 17 ), and serous endometrial cancer cells ( 18 ). The IND for ONC206 was accepted by the FDA and the first-in-human clinical trial ( Clinicaltrials.gov NCT04541082) with a starting dose of 90 mg in biomarker-defined adult recurrent and rare central nervous system tumors was initiated ( 13 ) and is currently recruiting patients.…”

Section: Introductionmentioning

confidence: 99%

A Novel Therapeutic Mechanism of Imipridones ONC201/ONC206 in MYCN-Amplified Neuroblastoma Cells via Differential Expression of Tumorigenic Proteins

et al. 2021

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Neuroblastoma is the most common extracranial nervous system tumor in children. It presents with a spectrum of clinical prognostic measures ranging from benign growths that regress spontaneously to highly malignant, treatment evasive tumors affiliated with increased mortality rates. MYCN amplification is commonly seen in high-risk neuroblastoma, rendering it highly malignant and recurrence prone. In our current study, we investigated the therapeutic potential of small molecule inducers of TRAIL, ONC201, and ONC206 in MYCN-amplified IMR-32 and non-MYCN-amplified SK-N-SH human neuroblastoma cell lines. Our results exhibit potent antitumor activity of ONC201 and ONC206 via a novel inhibition of EGF-induced L1CAM and PDGFRβ phosphorylation in both cell lines. Drug treatment significantly reduced cellular proliferation, viability, migration, invasion, tumorsphere formation potential, and increased apoptosis in both cell lines. The protein expression of tumorigenic NMYC, Sox-2, Oct-4, FABP5, and HMGA1 significantly decreased 48 h post-drug treatment, whereas cleaved PARP1/caspase-3 and γH2AX increased 72 h post-drug treatment, compared with vehicle-treated cells in the MYCN-amplified IMR-32 cell line. We are the first to report this novel differential protein expression after ONC201 or ONC206 treatment in human neuroblastoma cells, demonstrating an important multitarget effect which may yield added therapeutic benefits in treating this devastating childhood cancer.

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Section: Introductionmentioning

confidence: 99%

A Novel Therapeutic Mechanism of Imipridones ONC201/ONC206 in MYCN-Amplified Neuroblastoma Cells via Differential Expression of Tumorigenic Proteins

et al. 2021

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show abstract

Correction: Hu, W., et al. Targeting Dopamine Receptor D2 by Imipridone Suppresses Uterine Serous Cancer Malignant Phenotype. Cancers 2020, 12, 2436

Abstract: In the original article, there was a mistake in Figure 2B as published [...]

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A Novel Therapeutic Mechanism of Imipridones ONC201/ONC206 in MYCN-Amplified Neuroblastoma Cells via Differential Expression of Tumorigenic Proteins

A Novel Therapeutic Mechanism of Imipridones ONC201/ONC206 in MYCN-Amplified Neuroblastoma Cells via Differential Expression of Tumorigenic Proteins

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